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SKIN TEST

FACULTY OF MEDICINE MALANG ISLAMIC UNIVERSITY. SKIN TEST. Applying the tuberculin skin test. Courtesy of Dr. Marc Steben. Applying the tuberculin skin test. Applying the tuberculin skin test. Courtesy of Dr. Marc Steben. Reading the tuberculin skin test.

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SKIN TEST

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  1. FACULTY OF MEDICINE MALANG ISLAMIC UNIVERSITY SKIN TEST

  2. Applying the tuberculin skin test Courtesy of Dr. Marc Steben The MTCT-Plus Initiative

  3. Applying the tuberculin skin test The MTCT-Plus Initiative

  4. Applying the tuberculin skin test Courtesy of Dr. Marc Steben The MTCT-Plus Initiative

  5. Reading the tuberculin skin test • Read 2-3 days after placing the test • Feel for induration • Color change without induration is not included in the measurement • Use a ruler or calipers • Have someone else check if unsure • Always document the exact size (mm) – not just “positive” or “negative” The MTCT-Plus Initiative

  6. Reading the tuberculin skin test Courtesy of Dr. Marc Steben The MTCT-Plus Initiative

  7. Reading the tuberculin skin test The MTCT-Plus Initiative

  8. Y Y REAKSI HIPERSENSITIVITAS

  9. Hipersensitivitas adalah suatu reaksi yang tidak diharapkan dari respon imun tubuh. • Coombs dan Gell membagi menjadi 4 tipe (mekanisme dan waktu): • Rx. Hipersensitivitas tipe I • Rx. Hipersensitivitas tipe II • Rx. Hipersensitivitas tipe III • Rx. Hipersensitivitas tipe IV

  10. 4 types of hypersensitivity reactions (hives) Allergies

  11. Immune complex disease Delayed-type hypersensitivity

  12. Reaksi Hipersensitivitas tipe I • Reaksi Hipersensitivitas tipe cepat atau anafilaktik • Diperantarai IgE • Alergenproduksi IgE berikatan spesifik dengan reseptor di permukaan sel mast dan basofil  tersensitisasi • Kontak berikutnya  sederetan reaksi biokimia  degranulasi dan pelepasan mediator2 (histamin, leukotrien dan sitokin)  reaksi alergi • 15-30 menit setelah terpapar antigen, kadang keterlambatan (10-12 jam) • Dapat melibatkan kulit (urtikaria dan eksema), mata (konjungtivitis), nasofaring (rinitis), jaringan bronkopulmoner (asma), dan GI tract (gastroenteritis)

  13. Reaksi Hipersensitivitas tipe I………. • Contoh: reaksi anafilaksis terhadap bisa hewan, hay fever, urtikaria akibat makanan, dermatitis atopik, rhinitis alergika, konjungtivitis, asma, dll • Gejala : ketidaknyamanan ringan sampai kematian • Berat ringan gejala dipengaruhi : • antibodi IgE • jumlah alergen • faktor-faktor lain yang dapat meningkatkan respon (infeksi virus dan polutan)

  14. Biologic effects of mediators

  15. Tes diagnostik • Skin test (prick dan intradermal) • Kadar total IgE dan IgE spesifik terhadap alergen yang dicurigai (ELISA)  IgE tinggi pada kondisi atopik Terapi: • Antihistamin, adrenalin, bronkodilator, kortikosteroid, menghindari paparan alergen dan immunoterapi

  16. Skin test for allergy Ragweed Control negative (saline) Control positve (histamine)

  17. Type I hypersensitivity reaction Capillary dilation CAUSES MECHANISM PATHOPHYSIOLOGY Antigen Ingestants Food Drugs Pollens Dusts Molds Injectants Drugs Stings Vaccines Serum Increased Blood Volume Release of chemical mediators : Histamine SRS-A Kinins Prostaglandins Allergen interacts with IgE on mast cell Exudation of Cell, fluid protein Increased Capillary permebiality Pressure of exudate Nerve irritation Constriction of smooth muscle 23

  18. Type I hypersensitivity reaction (continued) CLINICAL EXAMPLES MANIFESTATIONS • Respiratory tract • Upper “sinus headache” • itching of eyes • tearing, sneezing, • watery nasal discharge, • itching of nose, • throat irritation • Lungs wheezing, dyspnea, • dry cough, tightness in chest • Respiratory tract • Upper “sinus headache” • itching of eyes • tearing, sneezing, • watery nasal discharge, • itching of nose, • throat irritation • Lungs wheezing, dyspnea, • dry cough, tightness in chest Allergic rhinitis Conjunctivitis Asthma Gastrointestinal Glossitis, cardiospasm Nausea, vomitting Irritable bowel Diarrhea, pruritus ani Food allergies Atopic dermatitis Urticaria Skin Urticaria, pruritus, Angioedema, weeping erthematosus vesico-papular lessions 24

  19. Reaksi Hipersensitivitas tipe II • Reaksi hipersensitivitas sitotoksik • Waktu reaksi : menit - jam • Contoh: reaksi transfusi, drug-induced hemolytic anemia, granulositopenia, dan trombositopenia • Diperantarai IgM atau IgG dan komplemen • Fagosit dan sel K punya peran • Interaksi antigen-antibodi pd permukaan sel, IgM atau IgG dgn antigen yang juga merupakan bagian integral membran sel atau telah terserap atau menyatu menjadi membran. • Mengaktifkan sistem komplemen dan sel yang terlibat dihancurkan. • Terapi: anti-inflamasi dan agen immunosupresif

  20. Type II hypersensitivity reaction Erytrhrocyte hemolysis Susceptability to infections • Antigen interacts with body cell i.e : • Erythrocyte • Leucocyte • Platelet • Vascular endothelium Agranulocytosis Thrombocytopenia Vasculitis PATHOPHYSIOLOGY CAUSES MECHANISM CLINICAL EXAMPLES Antigen Transfusion reaction Erythroblastosis fetalis Drugs Autoantibodies Unknown Reaction of IgG or IgM antobody with antigen on cell Activates complement Hemolytic anemia Purpura Vesicular purpura 28

  21. Reaksi Hipersensitivitas tipe III • Reaksi hipersensitivitas kompleks imun / reaksi Arthus • 3-10 jam setelah terpapar antigen • Diperantarai kompleks imun (antigen-antibodi) • Antigen eksogen (bakteri, virus, atau parasit)/endogen (SLE) • Contoh: serum sickness,SLE,rx Arthus,lupus nephritis,RA,dll • Terbentuk kompleks antigen-antibodi (toksik terhadap jaringan di tempat mereka diendapkan seperti ginjal / paru-paru) infiltrasi dinding pembuluh darah kecil  aktivasi kaskade komplemen pelepasan bahan aktif secara biologis, termasuk faktor-faktor yang menarik sel-sel fagosit yang akan menfagositosis kompleks tersebut

  22. Type III hypersensitivity reactions (Arthus Reaction) - Ab-Ag Complexes Critical mediators appear to be C5a-receptor and FcgRIII--probably present on mast cells

  23. Type III hypersensitivity reaction PATHOPHYSIOLOGY CAUSES MECHANISM CLINICAL EXAMPLES Antigen Autoantibodies Drugs Serum Chemicals Foreign antigen Bacteria Virus Glomerulo-nephritis Antigen and antibody form an immune complex Tissue destruction Deposits on vessel walls or basement membrane Vasculitis Inflammation Arthus reaction Rheumatoid diseases Serum sickness 31

  24. Diagnosis: • Biopsi jaringan (endapan Ig dan komplemen) • Kompleks imun pada darah dan penurunan jumlah komplemen Terapi: • Anti-inflamasi

  25. Reaksi Hipersensitivitas Tipe IV • tipeseluler atau tipe lambat (delayed type hypersensitivity) • > 12 jam • Contoh klasik: reaksi tuberkulin (Mantoux) yang memuncak 48 jam setelah injeksi antigen • Contoh lain: dermatitis kontak, penyakit autoimun dan infeksi seperti tuberkulosis, lepra, granulomatosa, toksoplasmosis, dll

  26. Biological effects of Eosinophil mediators Late stage of an allergic response includes the recruitment of eosinophils and Th2 cells contrast with a DTH (type IV) response which includes infiltration of macrophages and Th1 cells

  27. Mekanisme perusakan melibatkan limfosit T dan monosit dan/atau makrofag • Sel t sitotoksik (Tc) menyebabkan kerusakan langsung sedangkan sel T helper (TH1) mensekresi sitokin  aktivasi Tc, makrofag serta monosit  kerusakan Diagnosis: • Mantoux test dan patch test Terapi: - Kortikosteroid dan agen imunosupresif

  28. Type IV hypersensitivity reaction PATHOPHYSIOLOGY CAUSES MECHANISM CLINICAL EXAMPLES Antigen Tuberculin Poison Ivy Chemical Fungi Transplanted organs Virus Release of : Lymphokines Migration inhibition factor Interferon Killer cells Transfer factor Contact dermatitis Graft vs host reactions Viral infection Autoallergic disease Sensitized Lymphocyte reacts with antigen Injury and destruction of target organ 37

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